Pulmonary inflammatory disease (PID) is a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is associated with an abnormal inflammatory response of the lungs to, for example, noxious particles (fine particles such as those found in smoke and haze, with a diameter of 2.5 micrometers or less).
Pulmonary inflammatory diseases comprise inflammatory asthma i.e. asthma at a severe stage, chronic obstructive disease (COPD) such as chronic bronchitis, obstructive bronchiolitis, emphysema, pulmonary fibrosis, cystic fibrosis, and the like.
In PID patients, there is a significant neutrophilic inflammation in the bronchial walls leading to progressive destruction of airways structures by the repeated productions of proteases and oxidants (oxygen reactive species). To date, marketed therapies are not able to adequately decrease or prevent this neutrophilic inflammation in PID patients. In particular, it is well know that inhaled or oral steroids display no efficiency against neutrophilic inflammation. For example, in a study conducted by S. Culpitt et al.: Am J Respir Crit Care Med. 160: 1635-1639 (1999), which was performed in COPD patients, it reports the lack of efficacy of high doses inhaled steroids in COPD-related neutrophilic inflammation and chemotactic agents for neutrophils (mainly IL-8 in humans).
In view of the ineffectiveness of current steroidal treatment in PID patients, there is a need for effective steroidal treatment to adequately decrease or prevent neutrophilic inflammation in PID patients.